Plants pre-infected with a mild variant of a virus frequently become protected against more severe variants of the same virus through the cross protection phenomenon first discovered in 1929. Despite its widespread use in managing important plant virus diseases, the mechanism of cross protection remains poorly understood. Superinfection exclusion (SIE) is a widely observed phenomena where the diverse plant viruses block the re-infection of host cells by the same or highly similar viruses. Recent considerable progress has significantly advanced our understanding of how cross-protection and closely related process of SIE works. A new mechanistic model postulates that, for plant RNA viruses like Turnip crinkle virus (TCV), SIE manifests a viral function that denies progeny viruses the chance of re-replicating their genomes in the cells of their parents. It was further proposed that SIE manifests a virus-encoded, evolutionarily conserved function that minimizes the proliferation of replication errors and this function is realized through concentration-dependent acceleration of polymerization of a replication protein e.g p28. Although primarily based on observations made with TCV, this new model could be broadly applicable to other viruses and offer novel targets for antiviral therapy.